Aberrant signaling by the androgen receptor contributes to the initiation and progression of prostate cancer. The involvement of molecular chaperones in the processes of folding, activation, trafficking, and transcriptional activity of the androgen receptor provide different points along the signaling axis where regulation of androgen receptor activity can be hijacked to provide growth signals for clonal selection in cancer progression. Evidence exists of abnormal chaperone expression that could contribute to the upregulation of AR activity in prostate tumors. Regardless of whether chaperones are involved in the causation of prostate carcinogenesis, molecular chaperones provide therapeutic targets for the treatment of prostate cancer.